The invention relates generally to treatments with β2-agonists, such as treating neural conditions caused by spinal cord injuries and other causes, such as degenerative diseases, and more particularly to drugs and treatment methods which enhance the recovery of locomotor function and neuromuscular strength following spinal cord injuries or which result from other neurological conditions.
The spinal cord often responds to injury with profound loss of neuronal tissue and functional capacity. This can lead to significant loss of locomotor function. The same result can be caused by various neural conditions, such as motor neuron degeneration (mnd). For this reason, an important goal of rehabilitation following spinal cord injury or in the treatment of neurological conditions is to increase neuromuscular strength and function.
Prior treatments of spinal cord injuries have not been shown to be fully satisfactory and accordingly, it is desireable to provide improved treatment methods which can speed the recovery of the victim of a spinal cord injury, such as speeding the recovery of locomotor function and neuromuscular strength. A variety of agents including free radical scavengers, cyclooxygenase inhibitors, lipopolysaccharides, several steroids, calcium chelators, hypothermia, x-irradiation as well as surgical implants, that contain growth factors, have been shown to promote recovery based on various animal experiments. (See, e.g., Albin, M. S., R. J. White, G. Acosta-Rua, and D. Yashon, 1968, Study of functional recovery produced by delayed localized cooling after spinal cord injury in primates, J. Neurosurg. 29:113–120; Cheng, H., Y. Coa, and L. Olson. 1996, Spinal cord repair in adult paraplegic rats: Partial restoration of hind limb function, Science 273:510–513; Guth, L., Z. Zhang, and E. Roberts, 1994, Key role for pregnenolone in combination therapy, that promotes recovery after spinal cord injury, Proc. Natl. Acad. Sci. USA 91:12308–12312; Haghighi, S. S. ED. Hall, X. Z. Geng, J. J. Oro. and G. C. Johnson, 1993, Therapeutic value of 21-aminosteriod U74389F in acute spinal cord injury, Neurol. Res. 15:321–326; Kalderon. N., and Z. Fuks. 1996, Severed corticospinal axons recover electrophysiologic control of muscle activity after x-ray therapy in lesioned adult spinal cord, Proc. Natl. Acad. Sci. USA 93:11185–11190; and Kudo. Y. K. Takeda, and K. Yamazaki, 1990, Quin2 protects neurons against cell death due to Ca2+ overload, Brain Res. 528:48–54, all incorporated by reference. However, these countermeasures may be incompletely effective, difficult to administer or costly. Because of such limitations, additional or alternative agents, particularly of a pharmacological nature, that can be used in spinal cord injured patients or patients suffering from neurological diseases are needed.
Accordingly, it is desireable to provide improved treatments for neural conditions resulting from injury and other causes.